DESCRIPTION (Applicant's Description-edited) There is considerable evidence that increased levels of serum and urinary estrogens are associated with an increased risk of breast cancer in postmenopausal women. The pathway by which endogenous estrogen is metabolized may also be important. Estradiol (E2) is metabolized to a major extent through estrone (E1). E1 is then metabolized through two main metabolic pathways; the 16-alpha-hydroxy pathway yields biologically active products, while the 2-hydroxy pathway yields metabolites which are essentially devoid of estrogen activity. It has been suggested that an elevated ratio of 16-alpha- hydroxylation to 2- hydroxylation as measured by the ratio of 16-alpha-- hydroxyestrone (16-alpha-OHE1) to 2-hydroxyestrone (2-OHE1) is associated with an increased risk of breast cancer. However, the epidemiologic data that address this hypothesis are sparse. Our main aim in this study is to determine whether the known differences in breast cancer risk between ethnic groups is reflected in differences in the ratio of 16-alpha-OHE1/2-OHE1 across these groups. We will study this using urine samples from female postmenopausal participants in a large multiethnic cohort study in Hawaii and Los Angeles. Our secondary aim is to study whether diet, reproductive factors and other breast cancer risk factors affect the ratio. If the ratio of 16- alpha- OHE1/2-OHE1 can predict breast cancer risk and if this ratio can be affected by dietary or other factors, then this could have significant implications for breast cancer prevention studies.